Multiple lines of evidence has established that contractile performance of cardiac tissue is governed by the intimate relationship between sarcomere length and calcium-myofilament activation (LDA) forming the basis of the Frank-Starling mechanism. In contrast, relaxation is governed by the competition between calcium-myofilament inactivation and the external restoring force associated with muscle strength and loading. In order to eliminate mechanical and electrical inhomogeneity of bulk tissue, prior studies of contractility have been performed in intact single myocytes, albeit at slack length (as no satisfactory method exists to alter length/load in this mode , or in chemically-skinned cells. To examine the effect of strength on the twitch contraction and relaxation of single ventricular myocytes with intact sarcolemma, we developed a novel technique enabling reversible gradation in the resting cell length of up to 15-18%. Our initial results show (1) that the relative effect of bathing calcium to augment shortening velocity varied with the cell length is consistent with the concept that myofilament-calcium activation is length/load-dependent. A stretch of resting cell length increases twitch amplitude and accelerates relaxation without changing the cytosolic calcium transient. Thus, a cytosolic calcium-dependence of relaxation at slack length can be overridden by the external restoring force associated with stretch, consistent with the concept of a length/load-dependence of relaxation in bulk cardiac muscle, and, moreover, stretch represents a principal determinant of relaxation over calcium-myofilament inactivation in tissue with "normal" calcium homeostasis.